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Identification of candidate genes for devil facial tumour disease tumourigenesis
Robyn L Taylor1, Yiru Zhang2, Jennifer P Schöning2,3
1School of Biological Sciences, University of Tasmania, Hobart, Tasmania, 7001, Australia.
Abstract:
Devil facial tumour (DFT) disease, a transmissible cancer where the infectious agent is the tumour itself, has caused a dramatic decrease in Tasmanian devil numbers in the wild. The purpose of this study was to take a candidate gene/pathway approach to identify potentially perturbed genes or pathways in DFT. A fusion of chromosome 1 and X is posited as the initial event leading to the development of DFT, with the rearranged chromosome 1 material now stably maintained as the tumour spreads through the population. This hypothesis makes chromosome 1 a prime chromosome on which to search for mutations involved in tumourigenesis. As DFT1 has a Schwann cell origin, we selected genes commonly implicated in tumour pathways in human nerve cancers, or cancers more generally, to determine whether they were rearranged in DFT1, and mapped them using molecular cytogenetics. Many cancer-related genes were rearranged, such as the region containing the tumour suppressor NF2 and a copy gain for ERBB3, a member of the epidermal growth factor receptor family of receptor tyrosine kinases implicated in proliferation and invasion of tumours in humans. Our mapping results have provided strong candidates not previously detected by sequencing DFT1 genomes.
Insights
Devil facial tumour (DFT) disease, a contagious cancer threatening Tasmanian devils, was studied to find key genetic changes. Researchers identified rearrangements in cancer-related genes, including NF2 and ERBB3, offering new insights into DFT development.
Area of Science:
- Genetics
- Cancer Biology
- Conservation Genetics
Background:
- Devil facial tumour (DFT) disease is a contagious cancer decimating Tasmanian devil populations.
- The transmissible cancer is caused by the tumour cells themselves, leading to a severe decline in wild devil numbers.
Purpose of the Study:
- To identify genes and pathways perturbed in DFT using a candidate gene/pathway approach.
- To investigate the role of chromosome rearrangements, particularly on chromosome 1, in DFT development.
- To explore potential genetic targets for understanding and combating DFT.
Main Methods:
- A candidate gene/pathway approach was employed, focusing on genes involved in human nerve cancers and general tumour pathways.
- Molecular cytogenetics was used to map selected genes and identify rearrangements within DFT1 genomes.
- Comparison of identified rearrangements with existing DFT genome sequencing data.
Main Results:
- Rearrangements were identified in several cancer-related genes within DFT1.
- Specifically, the tumor suppressor NF2 region showed rearrangements, and a copy gain of ERBB3 was observed.
- These findings provide strong genetic candidates not previously detected through genome sequencing.
Conclusions:
- The study identified specific gene rearrangements (NF2, ERBB3) in DFT, offering new insights into the disease's genetic underpinnings.
- These findings highlight the importance of chromosome 1 in DFT tumourigenesis and provide novel targets for future research.
- The identified genetic alterations contribute to understanding the molecular mechanisms driving this transmissible cancer.
